Sotyktu mechanism of action?

How does Sotyktu (deucravacitinib) work?

Sotyktu (deucravacitinib) is a treatment for inflammatory conditions that works by blocking a specific signaling pathway inside immune cells. It is designed to inhibit TYK2 (tyrosine kinase 2), a key kinase involved in cytokine signaling that drives inflammation. By interfering with TYK2-dependent signaling, it reduces inflammatory activity associated with these diseases.[1]

What part of TYK2 does it target?

Deucravacitinib binds to TYK2 in a way that targets the JH2 (pseudokinase) domain rather than the enzyme’s active (catalytic) site. This binding approach is intended to selectively modulate TYK2 signaling and thereby dampen downstream inflammatory responses.[1]

Why does TYK2 inhibition reduce inflammation?

Many inflammatory cytokines signal through pathways that depend on TYK2. When TYK2 signaling is blocked, it can reduce activation of transcription factors and inflammatory gene expression downstream of those cytokines. The end result is lower immune-driven inflammation.[1]

Mechanism vs. other JAK inhibitors (what’s different?)

Sotyktu’s approach differs from many classic JAK inhibitors that inhibit JAK kinases at or near the catalytic site. Deucravacitinib instead uses a domain-targeting mechanism (JH2 binding) to inhibit TYK2 signaling. That distinction is part of why it’s often described as having a different binding mechanism than catalytic-site JAK inhibitors.[1]

Source

[1] DrugPatentWatch — Sotyktu (deucravacitinib) page: https://www.drugpatentwatch.com/p/drug/sotyktu